Enterobacter

Although sometimes regarded as rather worrisome pathogens,
Enterobacter species are not necessarily all bad. Not often a problem
in healthy individuals, they are opportunistic pathogens in people
with precarious immune systems, especially in hospitals where infection
control has broken down.

Significance to man

Benefits

Enterobacter cloacae has been used in biological control of plant diseases
(notably the seed-rotting oomycete Pythium ultimum).
Transgenic (aargh!?) E. cloacae have been used to control insect
pests on mulberry leaves [J Appl Microbiol 2000 Jan;88(1):90-97].

Harm

Enterobacter infections are becoming more common in intensive care. They
are mainly found where:

Substantially compromised patients are present - the very young,
the very old, and, especially, those with severe underlying disease,
such as neoplasms, or immune suppression including human immunodeficiency
virus infection - usually in the later stages of the disease.
[J Chemother 2001 Apr;13(2):195-201]

Enterobacter infection has also been traced to contaminated albumin
concentrates
(yet another reason not to use albumin),
prefilled saline syringes,
multidose vials
and contaminated
infant formulae (in the tin), with consequent necrotising enterocolitis.
[J Clin Microbiol 2001 Jan;39(1):293-297]
Total parenteral nutrition solutions have been contaminated during
preparation.
Haemodialysis machines with defective waste-handling ports have also
been responsible for haematogenous infection.
Strains have even been found that can grow in drinks containing
methylparaben (and will even grow in concentrations of 3000mg/L)!
Enterobacter meningitis in adults has been
reported following neurosurgery, presumably consequent on the usual
predisposing causes!

Mechanisms of injury

These have been poorly studied. See [J Antimicrob Chemother 1998 Mar;41(3):367-72]
for some data on aerobactin production, haemagglutinins (mannose-sensitive),
and resistance to serum bactericidal activity. A haemolytic leukotoxin
has been reported [Biochem Biophys Res Commun 2000 Aug 11;274(3):649-654].

Identification and features

A member of the family 'Enterobacteriaceae' (but not the 'type genus' - this
dubious honour belongs to Escherichia), Enterobacter can more-or-less
be identified if you encounter large lactose-fermenting colonies of Gram negative
rods, that are either raised or mucoid . The only important confounding bug
is Klebsiella, which is similar (and closely related) - admittedly,
Hafnia alvei is similar, but is rarely a cause of disease in
man. Serratia marcescens doesn't ferment lactose.

We can often distinguish Enterobacter from Klebsiella by seeing whether
the organism is motile - if it is, it must be Enterobacter (although
some are immotile). Enterobacter can also decarboxylate ornithine,
something Klebsiella cannot do.

Media

Eosin methylene blue (EMB) agar is selective for gram negative bacteria.
Enterobacter and Klebsiella form large mucoid colonies that are pink
to purple because of their lactose fermentation. They don't have the
metallic sheen of E. coli.
On MacConkey agar lactose fermentation results in a red colour.

Here are some pictures off the web:

Fig 1.

Fig 2.

Fig 3.

Fig 1. shows the red colour developed on MacConkey agar, Fig 2.
the organism growing on EMB agar, which you may contrast with Fig 3.
where you can see the greenish sheen of E. coli. The
References section gives the web sources of the pictures!

Species, Nomenclature and Relatives

There are several Enterobacter species, but E. cloacae and to
a lesser degree, E. aerogenes,
are the commonest pathogens. E. sakazakii (which forms bright yellow
colonies) is less common, but a nasty cause of neonatal sepsis, and
especially, meningitis, with brain abscesses, marked ventriculitis, and
hydrocephalus as a frequent consequence.
The rather unusual 'E. agglomerans' is now known as Pantoea agglomerans (also once called Erwinia milletiae) - it
may cause infection in ICU and has also been invoked as the cause for
"cotton fever" - encountered where intravenous drug abusers filter their
heroin with cotton!
(Other species are E. amnigenus, asburiae,
cancerogenus* [=taylorae =cancerogena =CDC enteric group 19], dissolvens, gergoviae,
hormaechei [=CDC enteric group 75], intermedius [=intermedium],
kobei [=NIH group 21],
nimipressuralis, and pyrinus*, possibly even 'cowanii' [=NIH group 42];
*=plant pathogens).

Different species of Enterobacter are differentiated by their
ability to ferment particular sugars, and possession of arginine dihydrolase,
lysine and ornithine decarboxylase.

Treatment

Carbapenems are at present probably the treatment of choice, although
cefepime may be used. Quinolone sensitivity is variable, and resistance
may develop during treatment (this can also occur with carbapenems).
Some organisms are sensitive to co-trimoxazole.

Note that some advocate combination chemotherapy for E. cloacae
infection.

Resistance

Resistance to everything apart from carbapenems (imipenem, meropenem)
and possibly quinolones is common. Some recommend that quinolones
not be used owing to emergence of resistance during therapy.
In fact, resistance to carbapenems may also emerge. Patterns and
rates of resistance vary greatly between antibiotics

Do NOT use
first, second or third generation cephalosporins as they are often
ineffective, and resistance commonly appears, especially in units
where cross-infection is common, and use of these agents is widespread.
Cefepime resistance is not at present a major problem, so this is
another option. (Cefepime and cefpirome resistance is now well-documented,
related to massive production of a modified cephalosporinase
[FEMS Microbiol Lett 2001 Feb 20;195(2):185-190] ).

Amp-C (stably derepressed) cephalosporinases are commonly present.

ESBL resistance may be transferred from Enterobacter to E. coli

E. cloacae resistance to carbapenems has been reported related to
a combination of:

loss of a major porin;
(As both beta lactams and fluoroquinolones enter Enterobacter species
through their F porin, loss of this protein might be expected to confer
resistance)

a group-1 beta lactamase mopping up any small amounts of
drug that get through;

Occasional resistance to carbapenems may be due to production of zinc
metallo-proteinases (e.g. IMP-1), or rarely 'Ambler class A' beta lactamases
(E. cloacae strain NOR-1).

As expected, mutations in DNA gyrase confer fluoroquinolone
resistance
- a single point mutation is enough.

Cautions

Avoid the use of first, second or third-generation cephalosporins,
as these may predispose to Enterobacter infections. Hand-washing
is still the most important way to prevent Enterobacter infection.

References

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